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cardiology first year drugs > cardio drugs > Flashcards

cardio drugs Flashcards

1
Q

moA of ivabradine

A

selective blocker of HCN channels, reduces the slope of pacemaker potential - slow HR reduces oxygen consumption

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2
Q

what is ivabradine used to treat

A

angina, tachycardia, mild to moderate chronic heart failure

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3
Q

side effects of ivabradine

A

arrhythmias and hypotension

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4
Q

what are dobutamine, adrenaline and Noradrenaline

A

b - adrenoceptor agonists

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5
Q

moA of b - adrenoceptor agonists

A

results in stimulation of adenylyl cyclase and production of cAMP which generates protein kinase A. Phosphorylation increases Ca influx and release of Ca from sacroplasmic reticulum increase contractility, force and rate and decrease cardiac efficiency

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6
Q

when are beta adrenoceptors used

A

in infarction, cariogenic shock, cardiomyopathy, inotropic support, heart failure (dobutamine), asthma emergency (adrenaline), anaphylactic shock

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7
Q

SE of beta adrenoceptors

A

arrhythmias and acute MI

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8
Q

what is dobutamine

A

selective for B 1

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9
Q

b1 selective b blockers

A

metoprolol, atenolol

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10
Q

what are propanolol, metoprolol, atenolol

A

beta blockers

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11
Q

MoA of beta blockers

A

decrease HR, contractility, MAP and O2 consumption

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12
Q

when are beta blockers used

A

angina, hypertension, heart failure, thyrotoxicosis

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13
Q

SE of beta blockers

A

asthma, fatigue, cold peripheries, HF - in patients with cardiac failure who rely on sympathetic drive to maintain CO, bradycardia and hypoglycaemia

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14
Q

what is atropine

A

a muscularinic antagonist

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15
Q

what does atropine do

A

it is non selective for M2 receptors and increases HR

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16
Q

when to use atropine

A

reverse bradycardia following MI, adjunct to anaesthesia, anti cholinesterase poisoning (reduces parasympathetic)

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17
Q

SE of atropine

A

arrhythmias, hallucinations, confusion

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18
Q

what is digoxin

A

a cardiac glycoside

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19
Q

Moa of digoxin

A

competes with K at alpha submit and blocks the Na/K pump

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20
Q

what does digoxin cause

A

increased contractility bu blocking the sarcolemma ATPase, indirectly increases vagal activity slowing SA node discharge and directly shortens action potential and refractory period increasing force, contraction and CO - effects are dangerously enhanced with hypokalaemia

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21
Q

when to use digoxin

A

HF, AF

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22
Q

SE of digoxin

A

Heart block, dysrhythmias, myocarditis

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23
Q

what is levosimendan

A

calcium sensitizer

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24
Q

moA of levosimendan

A

binds to troponin C in myocytes sensitising them to Ca

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25
Q

when to use levosimendan

A

acutely decompensated congestive heart failure and increased contractility

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26
Q

SE of levosimendan

A

headaches, arrhythmias and hypokalaemia

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27
Q

what is flecainide

A

a class I antiarrhythmic

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28
Q

what does a class 1 antiarrhythmic do

A

acts on voltage gated Na channels reducing Na channel current

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29
Q

when is flecainide used

A

for rhythmic control

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30
Q

SE of flecainide

A

negative inotropic effects

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31
Q

what are beta adrenoceptors

A

class II antiarrythmics

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32
Q

examples of beta adrenoceptors

A

propanalol

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33
Q

what are class II antiarryhtmics used for

A

rate control

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34
Q

what is amiodorane and sotalol

A

class III antiarhymic

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35
Q

MoA of class iii antiarryhtmics

A

voltage gated K channels

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36
Q

what do class iii anti arrhythmics do

A

lead to action potential prolongation

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37
Q

when are class iii anti arrhythmics used

A

for rhythm control

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38
Q

class IV drug example

A

verapamil

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39
Q

Moa of verapamil

A

calcium channel blocker

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40
Q

what is verapamil used for

A

rate control

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41
Q

what are isorbide mononitrate and GTN spray

A

nitrates

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42
Q

what do nitrates do

A

mimic the effect of the endothelium, produce nitric oxide which is formed through influx of Ca activation of eNOS and L -argine and NO caused efflux of Ca producing hyper polarisation and relaxation, Endothelin is also produced

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43
Q

what do nitrates cause

A

venorelaxation (decreased preload and after load, CO maintained as HR increases arteriolar dilation and increased coronary blood flow

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44
Q

when to use nitrates

A

in angina and acute heart failure

45
Q

side effects of nitrates

A

headache, hypotension, tolerance is common

46
Q

what is lisinopril

A

an ACEi

47
Q

moA of ace inhibitor

A

block the conversion of angiotensin I to angiotensin II so aldosterone and ADH are not stimulated

48
Q

when to use acei

A

hypertension and HF

49
Q

SE of acei

A

dry cough, renal dysfunction ( bad with renal artery stenosis and good for diabetic neuphropathy), angionerurotic oedema, petal abnormalitys

50
Q

what do acei cause

A

vasodilation and arterial dilatation

51
Q

what is losartan

A

a ARB

52
Q

Moa of ARB

A

blocks angiotensin II receptors

53
Q

when are ARB used

A

hypertension and HF

54
Q

side effects of ARB

A

renal dysfunction, oedema, no cough, contraindicated in pregnancy

55
Q

what are amlodipine, verapamil and dltiazem

A

calcium antagonists

56
Q

what do calcium antagonists do

A

decrease conduction at SA and AV node and cause decrease in HR

57
Q

when are calcium antagonists used

A

in hypertension, angina and supra ventricular arrhythmias

58
Q

se of CCB

A

ankle oedema and bradycardia

59
Q

what is doxazosin

A

an alpha blocker

60
Q

Moa of doxazosin

A

block a adrenoceptors to case vasodilation

61
Q

when does doxazosin be used

A

hypertension and prostatic hypertrophy

62
Q

se of alpha blockers

A

postural hypotension

63
Q

what are minoxidil and nicroandil

A

k channel openers

64
Q

Moa of k channel openers

A

hyperpolarisation which switches off calcium channels, mediated by ATP and relaxation of vascular smooth muscle

65
Q

what are k channels openers used for

A

severe hypertension, angina

66
Q

se of k channels

A

tachycardia and salt and water retention

67
Q

what is bendrofluazide

A

thiazide diuretic

68
Q

Moa of thiazide diuretics

A

inhibit NaCL reabsorption in distal tubules by blocking NaCl co transporter

69
Q

when to use thiazide diuretics

A

hypertension

70
Q

se of diuretics

A

hypokalaemia, arrhythmias and fatigue

71
Q

what is furosemide

A

a loop diuretic

72
Q

Moa of loop diuretics

A

inhibit NaCl reabsorption in the thick ascending limb of loop of Henle

73
Q

what do diuretics cause

A

increase in Na, Cl and water and blood volume

74
Q

when to use furesmide

A

heart failure

75
Q

what are simvastin and atorvastatin

A

statins

76
Q

what is simvastatin

A

anticholesterol

77
Q

Moa of statins

A

blocks HMG- COA reductase which inhibits the formation of cholesterol and lower LDL and total cholesterol inflammation and stabilised atherosclerotic plaque decreases thrombosis

78
Q

when are statins used

A

hypercholesterolemia

79
Q

se of statins

A

used in caution with hypothyroidism and history of liver disease - causes myalgia, myopathy, myositis

80
Q

what are bezafibrate and gemfibrozil

A

fibrates

81
Q

Moa of fibates

A

agonist of nuclear receptors which enhance transcription of LPL which hydrolysis triglycerides to fatty acids and glycerol

82
Q

when to use vibrates

A

in high triglyceride levels

83
Q

se of fibres

A

myositis

84
Q

what are colestyramine, colestipol and colesevelam

A

bile acid binding resins

85
Q

what do bile acid binding resins do

A

inhibit cholesterol absorption but casing the excretion of bile salts resulting in more cholesterol to be converted to bile salts it binds bile to the intestine so its not absorbed in the duodenum and uses liver metabolism to cholesterol to compensate for it lost

86
Q

when ti use bile acid binding resins

A

to cause decreased absorption of triglycerides and increases LDL repepctor expression

87
Q

what do bile acid binding resins cause

A

GI tract irritation

88
Q

Moa of ezetimibe

A

inhibits transport proteins and reduces the absorption of cholesterol

89
Q

what does exetimide do

A

decreases LDL

90
Q

se of ezetimibe

A

diarrhoea, abdominal pian, headache contraindicated in breastfeeding

91
Q

what is warfarin

A

anticoagulant

92
Q

how should warfarin be administered

A

IV

93
Q

Moa of warfarin

A

blocks clotting factors 2,7, 9, 10 serine proteases glycoproteins precursors of active throbbing factors g carboxylase enzyme is stimulated by bit K and motifs the serine proteases anticoagilants act as fit K antagonists which prevents the production of mature factors

94
Q

when to use warfarin

A

DVT, PE, NSTEMI, AF

95
Q

Moa of heparin

A

binds to antithrombin iii increasing its affinity for serine proteases o greatly increase their rate of inactivation

96
Q

what does factor Xa do

A

activates thrombin IIa

97
Q

what does thrombin IIa d o

A

causes fibrin

98
Q

what does fibrin cause

A

blood clot

99
Q

what are dabigatran etexilate and rivaroxaban

A

orally active inhibitors

100
Q

what dp dabigatran and etecilate inhibit

A

thrombin

101
Q

what does rivaraxabn inhibit

A

factor Xa

102
Q

what are aspirin and clopidogrel

A

anti platelet

103
Q

moa of anti platelets

A

prevent new throbosis, blocks COX, inhibits formation of TXA2 which causes crosslinkig of platelets blocks ADP from binding to P2Y12 recpetorand formation of fibrin

104
Q

when to use antiplatelets

A

angina, acute MI, cerebral vascular incident and TIA

105
Q

se of antiplatets

A

haemorrhage anywhere, peptic ulcer and aspirin sensitivity in asthma patients

106
Q

what are streptokinase, tissue plasminogen activator , alteplace and duteplace

A

fibrinolytic drugs

107
Q

Moa of fibrinolytic drugs

A

fibrinolytic cascade opposes coagulation cascade, activate formation of plasmin to form plasminogen which lysis fibrin into fibrin fragments casing lysis of the cot

108
Q

when to use antifibrinolutics

A

STEMI, PE AND CVA a nd recogen occlude arteries

109
Q

se of fibrinolytic drugs

A

haemorrhage risk - controlled by tranexami acid which inhibits plasminogen activation

cardiology first year drugs (1 decks)

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